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To: Chairman of the Government Commission
Vice Prime Minister of Kyrgyz Republic, B. Silaev
c.c. Minister of Health
Minister of Environment
Bishkek, June 9, 1998
Have all the patients (>2000) really been poisoned?
During and immediately after the incident, there was a possibility for serious disease through (oral or dermal) contact with CN1 in the water and/or (possibly) HCN2 in the air. With the passing of time relevant exposure became less and less probable, because of the following reasons.
- dilution of the CN concentration in the soil and irrigation channels through flushing
- decomposing of CN in soil through natural processes (sun, rain, bacteria)
- combining of CN with metals to form stable complexes
- use of hypochlorite which destroys CN
When there is no relevant exposure, there is no potential for disease. It should be kept in mind that CN is a substance which occurs in many natural products, like certain roots, fruits (apricots!) and certain vegetables. Please keep in mind that this is a natural process. CN is also a part of vitamin B12 which is essential for human beings. The human body can thus get rid of CN and does so by converting it to thiocyanate. This is a rapid process, after one hour only 50% of the original concentration can be found in the blood, after the second hour 25%, after the third hour 12.5%, etc.
Only when there is massive exposure, a serious and potentially life threatening situation occurs. In such a situation serious symptoms occur rapidly, because of lack of oxygen in the brain and the heart. Only then symptoms like palpitations, convulsions and coma occur. Generally speaking, if a patient still lives after four hours he will recover, even serious exposure.
Without such a high concentration of CN in the body, symptoms are minor, if any, and will resolve quickly in the absence of exposure. Concentrations in the blood will also diminish quickly and symptoms will subside. The concentrations in the soil that have been found after a few days make it unlikely that so many patients were intoxicated.
This of course does not rule out that people have smelled the typical odour or have had dermal contact with CN some days after the accident. It should however be clear that no serious disease could have resulted from that exposure.
It is therefore also unrealistic to attribute the symptoms reported by the inhabitants of other villages, at a distance of some kilometres, to CN-intoxication. There is also no other potential route for CN e.g. via groundwater or via the air that could have resulted in their exposure.
Only in sandy soils a very small quantity of CN may reach groundwater. In clay CN is bound by metals to form stable complexes and/or decomposed by micro-organisms; thus it cannot reach groundwater. CN that as HCN has been released to the air will disperse rapidly and can never reach toxic concentrations at such distances. (See also previous remarks on HCN in air).
Aftereffects
There is no reason to be afraid of genetic or reproductive effects
of CN, especially at low doses, because CN is a substance which
is found in our food. There is thus a continuous (low) exposure,
depending on the diet. As has been mentioned previously, CN is rapidly
removed from the body by conversion to thiocyanate.
Treatment
The treatment schemes that we have seen seem appropriate and, especially
step 1 - amylnitrite, NaNO2 and thiosulfate - reflect the latest
international views on the treatment of cyanide intoxication. However,
they should be applied in serious cases and also immediately after
exposure. When used later they are not very useful and probably
not without risk.
Conclusions
It is unlikely that as many as 2000 (or more) patients have experienced
a cyanide intoxication, due to the absence of possibilities of relevant
exposure after the first few days. (See also previous remarks on
soil-concentrations). Knowing this, treatment schemes, although
clinically spoken correct, may have been applied too rigorously.
Aftereffects (genetic, reproductive, cancer) are not to be expected.
In stating that cyanide intoxication was not likely to be as wide spread as was felt by the patients or reported by the physicians, we should keep the following in mind:
- absence of information about the accident in the first few hours
- general knowledge among people and physicians that cyanide is a potent toxic compound
- overflow of patients at Barskoon outpatient department and resulting stream of patients to other hospitals
- through lack of information about precise nature of cyanide intoxication, no clear statements from physicians who is a patient and who is not
- therefore any patient with concern about his/her own health or the health of their children becomes concerned and seeks medical advice
This pattern we have seen in Holland quite often. When there was a lack of information.
Recommendations
- Make plan for risk communication, local newspaper, mass media etc.
- Give information about nature of cyanide intoxication and absence of possibilities for further exposure.
- Make clear that the lake and fish are safe. CN does not build up in fish.
- Make clear that animals and animal products are safe. If necessary state that CN cannot build up in animals, because it is either broken down quickly or animals are dead immediately after exposure.
- Open information centre where everybody can go with questions about health, food products or other.
- Consider making emergency plans for factories in the vicinity of cities.
| WHO expert WHO expert |
Rob Cleven Mark van Bruggen |
1 CN is the cyanide ion.
2 HCN is hydrogen cyanide, a product
formed when sodium cyanide mixes with water. (Also known as hydrocyanic
acid and prussic acid.)